免疫球蛋白E
断点群集区域
B细胞受体
免疫学
抗体
抗原
等离子体电池
生物
锡克
克隆(Java方法)
受体
23号公路
B细胞
贪婪
分子生物学
生物化学
酪氨酸激酶
DNA
作者
Adam K. Wade-Vallance,Zhiyong Yang,Jeremy B. Libang,Marcus J. Robinson,David M. Tarlinton,Christopher D.C. Allen
摘要
The proper regulation of IgE production safeguards against allergic disease, highlighting the importance of mechanisms that restrict IgE plasma cell (PC) survival. IgE PCs have unusually high surface B cell receptor (BCR) expression, yet the functional consequences of ligating this receptor are unknown. Here, we found that BCR ligation induced BCR signaling in IgE PCs followed by their elimination. In cell culture, exposure of IgE PCs to cognate antigen or anti-BCR antibodies induced apoptosis. IgE PC depletion correlated with the affinity, avidity, amount, and duration of antigen exposure and required the BCR signalosome components Syk, BLNK, and PLCγ2. In mice with a PC-specific impairment of BCR signaling, the abundance of IgE PCs was selectively increased. Conversely, BCR ligation by injection of cognate antigen or anti-IgE depleted IgE PCs. These findings establish a mechanism for the elimination of IgE PCs through BCR ligation. This has important implications for allergen tolerance and immunotherapy as well as anti-IgE monoclonal antibody treatments.
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